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256 BASIC SKILLS IN INTERPRETING LABORATORY DATA
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copper accumulation in these organs eventually leads to irreversible damage such as cirrhosis and neurologic impairment.
66
Hypercupremia
Copper excess, or hypercupremia, is not common in humans and
usually occurs with a deliberate attempt to ingest large quantities
of copper. e exact amount of copper that results in toxicity is
unknown. Acute or long- term ingestion of >15 mg of elemental
copper may lead to symptomatic copper poisoning.67 Also, it has
been reported that drinking water with 2 to 3 mg/L of copper is
associated with hepatotoxicity in infants. Similar to other metallic poisonings, acute copper poisoning leads to nausea, vomiting,
intestinal cramps, and diarrhea.67 A larger ingestion can result in
shock, hepatic necrosis, intravascular hemolysis, renal impairment, coma, and death. Elevated intrahepatic copper concentrations may be present in patients with primary biliary cirrhosis
and biliary atresia.68 Long- term parenteral nutrition (PN) use
is also a risk factor for hepatic copper overload due to chronic,
unregulated exposure of IV copper through the multitrace element mixture. For patients receiving chronic home parenteral
nutrition, it is recommended that serum copper concentration
is monitored to prevent copper toxicity.
69,70
Chronic cholestasis
secondary to parenteral nutrition–associated liver disease has
been suggested as the primary cause. Because copper plays an
important role in the neurologic system, it has been suggested
that copper- induced free radical–induced neurodegeneration
may be a contributing factor for Alzheimer disease. At present,
there is no known treatment for hypercupremia.
Zinc
Normal range: 50 to 150 mcg/dL (7.7 to 23 micromol/L) serum
or plasma
Physiology
Next to iron, zinc is the most abundant trace element in the
body. It is an essential nutrient that is a constituent of, or a cofactor to, many enzymes. ese metalloenzymes participate in the
metabolism of carbohydrates, proteins, lipids, and nucleic acids.
As such, zinc inuences the following processes71:
• Tissue growth and repair
• Cell membrane stabilization
• Bone collagenase activity and collagen turnover
• Immune response, especially T- cell–mediated response
• Sensory control of food intake
• Spermatogenesis and gonadal maturation
• Normal testicular function
e normal adult body contains 1.5 to 2.5g of zinc. Aside
from supplementation with zinc capsules, dietary intake is the
only source of zinc for humans. Food sources of zinc include
meat products, oysters, and legumes. Food- based zinc is largely
bound to proteins and released by gastric acid and pancreatic
enzymes. Ionic zinc found in zinc supplements is absorbed in
the duodenum directly. Foods rich in calcium, dietary ber, or
phytate may interfere with zinc absorption, as can folic acid
supplements.
Aer absorption, zinc is transported from the small intestine to the portal circulation where it binds to proteins such as
albumin, transferrin, and other globulins. Circulating zinc is
bound mostly to serum proteins; two- thirds are loosely bound
to albumin and transthyretin, while one- third is bound tightly
to α-2 macroglobulin.53 Only 2% to 3% (3 mg) of zinc is either
in free ionic form or bound to amino acids.
72,73
Zinc can be found in many organs. Tissues high in zinc
include liver, pancreas, spleen, lungs, eyes (retina, iris, cornea,
and lens), prostate, skeletal muscle, and bone. Because of their
mass, skeletal muscle (60% to 62%) and bone (20% to 28%) have
the highest zinc contents among the body tissues.71 Only 2% to
4% of total body zinc is found in the liver. In blood, 85% is in
erythrocytes, although each leukocyte contains 25 times the zinc
content of an erythrocyte.
71
Plasma or serum zinc concentration is a poor indicator of
total body zinc store. Because 98% of the total body zinc is
present in tissues and end organs, the plasma zinc concentration tends to reect the continuous shiing from intracellular sources (ie, zinc tracking). Additionally, metabolic stress,
such as infection, acute myocardial infarction, and critical illnesses increase intracellular shiing of zinc to the liver and
lower serum zinc concentrations, even when total body zinc is
normal. Conversely, plasma zinc concentrations may be normal
during starvation or wasting syndromes due to release of zinc
from tissues and cells.71 erefore, serum/plasma zinc concentration alone has little meaning clinically in patients with acute
illnesses. It has been suggested that the rate of zinc turnover in
the plasma provides better assessment of the body zinc status.
is may be achieved by measuring 24- hour zinc loss in body
uids (eg, urine and stool). However, this approach is rarely
practical for critically ill patients as renal failure is oen present. Alternatively, zinc turnover and mobilization may be determined by adjusting plasma zinc concentrations with serum α-2
macroglobulin and albumin concentrations.
72,73
To more accurately assess the body zinc status, others have suggested monitoring the functional indices of zinc, such as erythrocyte alkaline
phosphatase, serum superoxide dismutase, and lymphocyte 5′
nucleotidase. However, the clinical validity of these tests remains
to be substantiated, especially in patients who are acutely ill.
Zinc undergoes substantial enteropancreatic recirculation
and is excreted primarily in pancreatic and intestinal secretions. Diarrhea signicantly increases zinc loss. Zinc is also lost
dermally through sweat, hair and nail growth, and skin shedding. Except in certain disease states, only 2% of zinc is lost in
the urine.
Hypozincemia
In Western countries, zinc deciency is rare from dietary insufciency. Individuals with no acute illnesses whose serum zinc
concentrations are <50 mcg/dL (<7.6 mol/L) are at an increased
risk for developing symptomatic zinc deciency. It also must
be emphasized that serum zinc exhibits a negative acute phase
response. e presence of proinammatory cytokines causes
an intracellular and intrahepatic inux of zinc from the serum,
which would lead to transient hypozincemia. erefore, serum
or plasma zinc concentration alone should not be used to assess
CHAPTER 11 • ElECTRolyTEs, oTHER MinERAls, And TRACE ElEMEnTs 257
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zinc status in patients with acute illnesses or any acute inammatory response. Given the caveats of measuring serum zinc
concentrations in certain disease states, response to empirical
zinc supplementation may be the only way of diagnosing this
deciency. In the presence of chronic diseases, it is dicult to
determine if zinc deciency is clinical or subclinical because of
the reduced protein binding. Conditions leading to deciency
may be divided into ve classes (Tabl e 11-12):
• Low intake
• Decreased absorption
• Increased use
• Increased loss
• Unknown causes
Zinc deciency is commonly caused by diarrhea and insufcient intake. Patients with increased ostomy output due to GI
tract surgery are especially at risk for zinc deciency. Acrodermatitis enteropathica is an autosomal, recessive disorder
involving zinc malabsorption that occurs in infants of Italian,
Armenian, and Iranian heritage. It is characterized by severe
dermatitis, chronic diarrhea, emotional disturbances, and
growth retardation.71 Examples of malabsorption syndromes
that may lead to zinc deciency include Crohn disease, celiac
disease, and short bowel syndrome.
Excessive zinc may be lost in the urine (hyperzincuria),
as occurs in alcoholism, beta thalassemia, diabetes mellitus,
diuretic therapy, nephrotic syndrome, sickle cell anemia, and
treatment with parenteral nutrition. Severe or prolonged diarrhea (eg, inammatory bowel diseases and GI gra versus host
disease) may lead to signicant zinc loss in the stool. Patients
with end- stage liver disease frequently have depleted zinc storage due to decreased functional hepatic cell mass.
Because zinc is involved in a diverse group of enzymes, its
deciency manifests in numerous organs and physiologic systems (Table11-13). Dysgeusia (lack of taste) and hyposmia
(diminished smell acuity) are common. Pica is a pathologic
craving for specic food or nonfood substances (eg, geophagia).
Chronic zinc deciency, as occurs in acrodermatitis enteropathica, leads to growth retardation, anemia, hypogonadism, hepatosplenomegaly, and impaired wound healing. Additional signs
and symptoms of acrodermatitis enteropathica include diarrhea;
vomiting; alopecia; skin lesions in oral, anal, and genital areas;
paronychia; nail deformity; emotional lability; photophobia;
blepharitis; conjunctivitis; and corneal opacities.
TABLE 11-12. Etiologies of Zinc Deciency
Low intake
Anorexia
Nutritional deciencies
Alcoholism
CKD
Premature infants
Certain vegetarian diets
Exclusion of trace elements in parenteral nutrition
Decreased absorption
Acrodermatitis enteropathica
Malabsorption syndromes
Bariatric surgery
Short bowel syndrome
Increased use
Adolescence
Lactation
Pregnancy
Increased loss
Alcoholism
β- thalassemia
Cirrhosis
Diabetes mellitus
Diarrhea
Diuretic therapy
Enterocutaneous stula drainage
Exercise (longGlucagon
Impaired enteropancreatic recycling
Nephrotic syndrome
Protein- losing enteropathies
Sickle cell disease
Unknown causes
Arthritis and other inammatory diseases
Down syndrome
term, strenuous)
Hyperzincemia
Zinc is one of the least toxic trace elements. Clinical manifestations of excess zinc, hyperzincemia, occur with chronic, high
doses of a zinc supplement. However, patients with Wilson disease who commonly take high doses of zinc rarely show signs
of toxicity. is may be explained by the stabilization of serum
zinc concentrations during high- dose administration. As much
as 12g of zinc sulfate (>2,700 mg of elemental zinc) taken over
2 days has caused drowsiness, lethargy, and increased serum
lipase and amylase concentrations. Nausea, vomiting, and diarrhea also may occur.
71
Manganese
Normal range: Varies depending on assay method, sample
(whole blood versus serum), and age. Whole blood method
is preferred to detect toxicity. Normal whole blood manganese
concentrations range from 4 to 15 mcg/L (72 to 270 nmol/L)
Physiology
Manganese is an essential trace element that serves as a cofactor
for numerous diverse enzymes involved in carbohydrate, protein, and lipid metabolism; protection of cells from free radicals;
steroid biosynthesis; and metabolism of biogenic amines.74 Interestingly, manganese deciency does not aect the functions of
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TABLE 11-13. Signs and Symptoms of Zinc
Deciency
Signs
Acrodermatitis enteropathica
Anemia
Anergy to skin test antigens
Complicated pregnancy
Excessive bleeding
Maternal infection
Premature or stillborn birth
Decreased basal metabolic rate
Decreased circulating T
Decreased lymphocyte count and function
Effect on fetus, infant, or child
Congenital defects of skeleton, lungs, and CNS
Fetal disturbances
Growth retardation
Hypogonadism
Impaired neutrophil function
Impairment and delaying of platelet aggregation
Increased susceptibility to dental caries
Increased susceptibility to infections
Mental disturbances
Pica
Poor wound healing
Short stature in children
Skeletal deformities
Symptoms
Acne and recurrent furunculosis
Ataxia
Decreased appetite
Defective night vision
Hypogeusia
Hyposmia
Erectile dysfunction
Oral ulcers
T4 = thyroxine.
concentration
4
manganese because animal tissues have low contents. Manganese is absorbed from the small intestine by a mechanism
similar to that of iron. However, only 3% to 4% of the ingested
manganese is absorbed. Dietary iron and phytate may aect
manganese absorption.
77
Human and animal tissues have low manganese content.
Tissues relatively high in manganese are the bone, liver, pancreas, and pituitary gland. Most circulating manganese is loosely
bound to the β-1 globulin transmanganin, a transport protein
similar to transferrin. With overexposure, excess manganese
accumulates in the liver and brain, causing severe neuromuscular signs and symptoms.
Manganese is excreted primarily in biliary and pancreatic
secretions. In manganese overload, other GI routes of elimination also may be used. Little manganese is lost in urine.
Manganese Deficiency
Because of its relative abundance in plant sources, manganese
deciency is rare among the general population. Deciency
normally occurs aer several months of deliberate manganese
omission from the diet. Little is known regarding serum manganese concentrations and the accompanying disease states
in humans.78 Limited evidence suggests that manganese deciency may be associated with bone demineralization and poor
growth in children, skin rashes, hair depigmentation, decreased
serum lipids, depression, and increased premenstrual pain in
women.
79,80
Manganese Excess
Manganese is one of the least toxic trace elements. Overexposure
primarily occurs from inhalation of manganese compounds (eg,
manganese mines).77 Long- term use of parenteral nutrition is a
risk factor for hypermanganesemia caused by continued and
unregulated exposure. e excess amount accumulates in the
liver and brain, resulting in severe neuromuscular manifestations. Patients receiving home parenteral nutrition with trace
elements daily for >6 months should have serum manganese
concentration monitored.
alopathy and profound neurologic disturbances that mimic
Parkinson disease.
84-86
because metabolism of biogenic amines is altered in both manganese excess and Parkinson disease. Other signs and symptoms include anorexia, apathy, headache, erectile dysfunction,
and speech disturbances. Inhalation of manganese products may
cause manganese pneumonitis.
69,70,81-83
Symptoms include enceph-
ese manifestations are not surprising
77
most of these enzymes, presumably because magnesium may
substitute for manganese in most instances.74 In animals, manganese is required for normal bone growth, lipid metabolism,
reproduction, and CNS regulation.
75,76
Manganese plays an important role in the normal function of
the brain, primarily through its eect on biogenic amine metabolism. is eect may be responsible for the relationship between
brain concentrations of manganese and catecholamines.
e manganese content of the adult body is 10 to 20 mg.
Manganese homeostasis is regulated through control of its
absorption and excretion. Plants are the primary source of food
74,75
Selenium
Average range: Varies depending on assay method, sample
(whole blood versus serum), and age. Concentrations in blood
and urine reect recent selenium intake. Normal whole blood
selenium concentrations are typically between 150 and 240
ng/mL, typical normal serum selenium concentration is usually between 70 and 150 ng/mL for patients >1 year
Physiology
Selenium is a trace element that is naturally present in many
foods and available as a dietary supplement. e primary
CHAPTER 11 • ElECTRolyTEs, oTHER MinERAls, And TRACE ElEMEnTs 259
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physiologic role of selenium is to serve as an antioxidant, especially via the selenoprotein, glutathione peroxidase, to help
protect cells from oxidative damage. In most cases, selenoprotein and glutathione work along with other cellular antioxidant
defense mechanisms, such as ascorbate, tocopherol, and superoxide dismutase. Glutathione peroxidase activity is decreased in
patients with selenium deciency. Upon repletion of selenium,
glutathione activity is restored.
87
Selenium exists in the inorganic form (selenite) and organic
form (selenomethionine and selenocysteine). e most common form of selenium in the active site of glutathione peroxidase is selenocysteine, which has independent activity that does
not allow it to use hydrogen peroxide as a substrate. Selenomethionine is another common form of selenium in human cells.
e estimated dietary intake of selenium varies geographically due to dietary variance and characteristics of the soil. Food
sources of selenium include Brazil nuts, seafoods, organ meats,
breads, grains, poultry, and eggs. About 90% of selenium is
absorbed as the organic form of selenomethionine in the human
body and is available in that form in most dietary supplements.
e injectable forms of selenium are selenious acid and sodium
selenite.
79,88
Selenium Deficiency
Dietary selenium deciency is rare in the United States and Canada and in isolation rarely causes illness. Patients with acute
inammation or uncontrolled chronic illnesses have lower selenium concentrations, likely due to increased oxidative stress
associated with their diseases. Critically ill patients have low
serum selenium concentration, and the magnitude of deciency correlates with the severity of illness. Supplementation
with large doses of antioxidant cocktail containing selenium has
not been shown to improve survival or decreased ICU or hospital length of stay.
89,90
Patients undergoing long- term hemodialysis and patients living with human immunodeciency virus
(HIV) are also likely to develop selenium deciency. For patients
undergoing hemodialysis, selenium is removed from the blood.
Due to uremia and dietary restrictions, patients may have low
dietary intakes that may be supplemented. However, little evidence suggests that supplementation is benecial in this patient
population.91 Patients living with HIV have low levels of selenium due to insucient intake and malabsorption due to GI
symptoms (ie, diarrhea). More evidence is needed to determine
whether selenium supplementation can reduce the risk of mortality, hospitalization, and HIV transmission.
92
Selenoproteins may help prevent oxidative modication
of lipids, thus reducing inammation and preventing platelet aggregation. However, it is yet to be determined if patients
should supplement with selenium as a primary prevention or if it
should be used as a tertiary prevention for patients who already
have cardiovascular disease. ere are some conicting reports
on whether selenium supplementation may increase the risk of
advanced prostate cancer and skin cancer in men.
93
Selenium Excess
Inorganic and organic forms of selenium can have similar toxic
eects. Tolerable upper intake levels for selenium vary based on
age and geographic location. Common symptoms of acute selenium excess include garlic breath odor and a metallic taste in
the mouth. For adults, serum selenium concentration >400 mcg
could produce symptoms such as hair and nail loss, GI and neurologic symptoms, acute respiratory distress syndrome, tremors,
kidney failure, and cardiac failure. Death from selenium toxicity is rare but can occur with excessive intake.
88,92
A case report
of fatality was associated with a single oral ingestion of 10g of
sodium selenite (96% purity) in a 75- year- old man. e patient
presented with cardiovascular collapse, hypoxemic respiratory
failure, mild hypokalemia (3.4 mEq/L), and a serum selenium
concentration of 5,370 ng/mL.
93
Chromium
Average range: serum chromium 0.3 to 0.9 ng/mL; sample
contamination (eg, use of regular blood collection tubes not
designed for trace elements) may result in ranges from 2 to
5ng/mL
Physiology
e main physiologic role of chromium is as a cofactor for insulin.94 In its organic form, chromium potentiates the action of
endogenous and exogenous insulin, presumably by augmenting its adherence to cell membranes.49 e organic form is in
the dinicotinic acid–glutathione complex or glucose tolerance
factor (GTF).79 Chromium is the metal portion of GTF; with
insulin, GTF aects the metabolism of glucose, cholesterol, and
triglycerides.94 erefore, chromium is important for glucose
tolerance, glycogen synthesis, amino acid transport, and protein synthesis. Chromium also is involved in the activation of
several enzymes
e adult body contains an average of 5 mg of chromium.95
Food sources of chromium include brewer’s yeast, spices, vegetable oils, unrened sugar, liver, kidneys, beer, meat, dairy products, and wheat germ.95 GTF is present in the diet and can be
synthesized from inorganic trivalent chromium (Cr+3) available
in food and dietary supplements.50 Chromium is absorbed via a
common pathway with zinc; its degree of absorption is inversely
related to dietary intake, varying from 0.5% to 2%.
Chromium circulates as free Cr3+, bound to transferrin and
other proteins, and as the GTF complex. GTF is the biologically
active moiety and is more important than total serum chromium concentration. Trivalent chromium accumulates in the
hair, kidneys, skeleton, liver, spleen, lungs, testes, and large intestine. GTF concentrates in insulin- responsive tissues such as the
79,94
liver.
e metabolism of chromium is not well- understood for several reasons:
• Low concentrations in tissues
•
Diculty in analyzing chromium in biological uids and tis-
sue samples
• Presence of dierent chromium forms in food
Homeostasis is controlled by release of chromium from GTF
and by dietary absorption. e kidneys are the main site of elimination, where urinary excretion is constant despite variability
in the fraction absorbed.
94
79,94
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Chromium Deficiency
It is important to stress that the body store of chromium cannot be reliably assessed. Serum or plasma chromium may not be
in equilibrium with other pools. As with other trace elements,
the risk for developing chromium deciency increases over
time with lack of oral intake and insucient supply from other
sources, such as a trace element- free parenteral nutrition solu-
69,70
tion.
Marginal deciencies or defects in use of chromium
may be present in elderly patients, patients with diabetes, or
patients with atherosclerotic coronary artery disease.
95
Hyperglycemia increases urinary losses of chromium. Coupled with marginal intake, a patient with type II diabetes is predisposed to chromium deciency, which can further impair
glucose tolerance.
94,96
Finally, multiparous women are at a higher
risk than nulliparous women for becoming chromium decient
because, over time, chromium intake may not be adequate to
meet fetal needs and maintain the mother’s body store.
e manifestations of chromium deciency may involve
insulin resistance and impaired glucose metabolism. Such mani
festations may present clinically in three stages as the deciency
progresses:
•
Glucose intolerance is present but is masked by a compensa-
tory increase in insulin release.
•
Impaired glucose tolerance and lipid metabolism are clini-
cally evident.
•
Marked insulin resistance and symptoms associated with
hyperglycemia are evident.
Chromium supplementation has been shown in patients with
diabetes to increase insulin sensitivity, improve glucose control,
and shorten the QTc interval, suggesting a potential favorable
eect on cardiovascular risk. However, currently, no conclusive
support demonstrates the benet of chromium supplementation in patients with diabetes or persons with impaired glucose
metabolism.
Chromium deciency may lead to hypercholesterolemia
and become a risk factor for developing atherosclerotic disease.
Low chromium tissue concentrations have been associated with
increased risk for myocardial infarction and coronary artery disease in both healthy subjects and patients with diabetes, although
a cause- and- eect relationship has not been established.
96
Chromium Excess
Chromium has low toxicity with no established specic clinical
symptoms or presentations. e clinical signicance of a high
body store of chromium is unknown. Patients receiving longterm home parenteral nutrition with a standard daily amount of
chromium from the multitrace element admixture may have an
increase serum chromium concentration; however, the clinical
risk is unknown at this point.69 Serum chromium concentrations may be increased in asymptomatic patients with metalon- metal prosthetics.
SUMMARY
Hyponatremia and hypernatremia may be associated with high,
normal, or low total body sodium. Hyponatremia may result
from abnormal water accumulation in the intravascular space
(dilutional hyponatremia), a decline in both extracellular water
and sodium, or a reduction in total body sodium with normal
water balance. Hypernatremia is most common in patients with
either an impaired thirst mechanism (eg, neurohypophyseal or
pituitary lesion) or an inability to replace water depleted through
normal insensible loss or from renal or GI loss. Neurologic manifestations are signs and symptoms oen associated with sodium
and water imbalance. e most common symptom of hyponatremia is confusion. However, if sodium continues to fall, seizures, coma, and death may result. irst is a common symptom
of hypernatremia; decreased urine specic gravity, suggesting
less concentrated urine, is oen observed.
Hypokalemia and hyperkalemia may indicate either a true
or an apparent (due to transcellular shiing) potassium imbalance. Hypokalemia can occur because of excessive loss from the
kidneys (diuretics) or GI tract (vomiting or diarrhea). e most
serious manifestation involves the cardiovascular system (ie, cardiac arrhythmias). Renal impairment, usually in the presence of
high intake, commonly causes hyperkalemia. Like hypokalemia,
the most serious clinical manifestations of hyperkalemia involve
the cardiovascular system.
Serum chloride concentration may be used as a conrmatory
test to identify abnormalities in uid and acid–base balance.
Hypochloremia may be diuretic induced and results from the
concurrent loss of sodium and also contraction alkalosis. Signs
and symptoms associated with these conditions are related to
the abnormalities in uid or acid–base balance and underlying
causes rather than to chloride itself.
Hypomagnesemia usually results from excessive loss from
the GI tract (eg, nasogastric suction, biliary loss, ileostomy or
chronic diarrhea) or the kidneys (eg, diuresis). Magnesium
depletion is usually associated with neuromuscular symptoms
such as weakness, muscle fasciculation with tremor, tetany, and
increased reexes. Increased magnesium intake in the presence of renal dysfunction commonly causes hypermagnesemia.
Neuromuscular signs and symptoms that are opposite to those
caused by hypomagnesemia may be observed.
e most common causes of true hypocalcemia are disorders of vitamin D metabolism and PTH production. Severe
hypocalcemia can be a medical emergency and lead to cardiac
arrhythmias and tetany, with symptoms primarily involving the
neuromuscular system.
e most common causes of hypercalcemia are malignancy
and primary hyperparathyroidism. Symptoms oen consist of
vague GI reports such as nausea, vomiting, abdominal pain,
anorexia, constipation, and diarrhea. Severe hypercalcemia can
cause acute neurologic changes and possibly cardiac arrhythmias, which can be a medical emergency.
The most common causes of hypophosphatemia are
decreased intake and increased renal loss. Although mild
hypophosphatemia is usually asymptomatic, severe depletion (<1 mg/dL or <0.32 mmol/L) is typically associated with
muscle weakness, rhabdomyolysis, paresthesia, hemolysis,
platelet dysfunction, and cardiac and respiratory failure. e
most common cause of hyperphosphatemia is renal dysfunction, oen with a GFR <25 mL/min. Signs and symptoms, if
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present, primarily result from the ensuing hypocalcemia and
hyperparathyroidism.
Hypocupremia is uncommon in adults but can occur in
infants, especially those born prematurely. Also susceptible are
infants who have chronic diarrhea or malabsorption syndrome
or whose diet consists mostly of milk. Prolonged hypocupremia
results in neutropenia and iron- deciency anemia that is correctable with copper.
Copper excess is not common and may result from a deliberate attempt to ingest large quantities. Similar to other metallic
poisonings, acute copper poisoning leads to nausea and vomiting, intestinal cramps, and diarrhea.
Likely candidates for zinc deciency are infants; rapidly growing adolescents; menstruating, lactating, or pregnant women;
persons with low meat intake; institutionalized patients; and
patients receiving parenteral nutrition solutions without trace
elements for prolonged periods. Because zinc is involved with
a diverse group of enzymes, its deciency manifests in dierent organs and physiologic systems. Zinc excess develops from
chronic, high- dose zinc supplementation. Signs and symptoms
include nausea, vomiting, diarrhea, drowsiness, lethargy, and
increases in serum lipase and amylase concentrations.
Manganese deficiency can occur after several months
of deliberate omission from the diet. Signs and symptoms
include weight loss, slow hair and nail growth, color change
in hair and beard, transient dermatitis, hypocholesterolemia,
and hypotriglyceridemia. Manganese excess primarily occurs
through inhalation of manganese compounds (eg, manganese
mines). As a result of manganese accumulation, severe neuromuscular manifestations occur, including encephalopathy and
profound neurologic disturbances, which mimic Parkinson disease. Inhalation of manganese products may cause manganese
pneumonitis.
Chromium deciency may be found in patients receiving
prescribed chronic nutrition regimens that are low in chromium
content. Insulin resistance and impaired glucose metabolism are
the main manifestations.
LEARNING POINTS
1.
What does an abn ormal serum electrolyte concentration
mean?
ANSWER: An isolated abnormal serum electrolyte concentra-
tion may not always necessitate immediate treatment because
it can be the result of a poor sample (hemolyzed blood sample),
wrong timing (during an IV infusion or immediately after hemodialysis), or other confounding factors. Careful assessment of
the patient’s existing risk factors, history of illness, and clini
cal symptoms should be made to correctly interpret a specic
laboratory result. Patients with abn ormal serum electrolyte concentrations who are also symptomatic, especially with potentially life- threatening clinical presentations such as EKG changes,
should be treated promptly. The cause or precipitating factor of
the electrolyte abnormality should be identied and corrected,
if possible.
2. How should we approach a patient who has an abn ormal
serum sodium concentration?
ANSWER: Alteration of serum sodium concentration can be pre-
cipitated by sodium alone (either excess or deciency) or abnormal water regulation. It is important to fully assess the patient’s
sodium and uid status, symptoms, physical exam ndings, and
medical, surgical, and medication history for factors that may
precipitate sodium disorders. Because the homeostasis of sodium
and water is closely regulated by the kidney, it may be useful
to check urine electrolytes and osmolality to help establish the
diagnosis and guide clinical management.
3.
What are the most common risk factors that can lead to
hyperkalemia?
ANSWER: The leading cause of hyperkalemia is renal function
impairment, especially acute renal insufciency and associated
metabolic acidosis common in severe acute kidney injury. Two
other important causes are drug- induced hyperkalemia (eg, ACE
inhibitors, potassium- sparing diuretic) and high dietary intake
(especially with CKD).
4.
What is the clinical signicance of abnormal serum cal
cium and phosphorus concentrations?
ANSWER: Severe hypocalcemia and hypercalcemia can result in
neuromuscular problems. In addition, signicant hypercalcemia
may cause EKG changes and arrhythmias. Although hyperphosphatemia is not expected to cause any acute problems, severe
hypophosphatemia can result in neurologic and CNS manifestations. In the presence of chronic hyperphosphatemia, especially
in patients with CKD, the risk is increased for phosphorus to bind
with calcium to form insoluble complexes that will result in soft
tissue and vascular calcication. There is an increasing amount
of evidence to show that such vascular calcication can increase
the mortality and morbidity of CKD patients. Concurrent hypercalcemia further increases the serum calcium–phosphate product
and exacerbates the calcication process.
5. What is the most common clinical presentation of hypo-
cupremia and what are the causes of copper deciency?
ANSWER: The most common clinical symptoms associated
with hypocupremia are neurologic symptoms, which may present as ataxia, spasticity, muscle weakness, peripheral neuropathy, loss of vision, anemia, and leukopenia. The most common
causes include intestinal malabsorption, post- bariatric surgery
status, and decreased nutrient consumption.
REFERENCES
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264 BASIC SKILLS IN INTERPRETING LABORATORY DATA
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QUICKVIEW | Sodium
PARAMETER DESCRIPTION COMMENTS
Common reference ranges
Adults 135-145 mEq/L (135–145 mmol/L) Useful for assessment of uid status
Pediatrics: premature neonates 128–148 mEq/L (128–148 mmol/L)
Pediatrics: older children 138–145 mEq/L (138–145 mmol/L)
Critical value >160 or <120 mEq/L (>160 or
<120 mmol/L)
Natural substance? Yes Most abundant cation in
Inherent activity? Yes Maintenance of transmembrane
Location
Storage Mostly in extracellular uid
Secretion/excretion Filtered by kidneys, mostly reabsorbed;
some secretion in distal nephron
Major causes of…
High results
Associated signs and symptoms Mostly neurologic
Low results Multiple (discussed in text) Can occur with low, normal, or high
Associated signs and symptoms Mostly neurologic
After insult, time to…
Multiple (discussed in text) Can occur with low, normal, or high
Acute changes more dangerous than
chronic abnormalities
extracellular uid
electric potential
Closely related to water
homeostasis
total body sodium
total body sodium
Initial elevation or positive result Hours to years, depending on
Peak values Hours to years, depending on
Normalization Days, if renal function is normal Faster with appropriate treatment
Drugs often monitored with test Diuretics, ACE inhibitors, aldosterone
Causes of spurious results None
chronicity
chronicity
antagonists, angiotensin II antagonists,
ADH analogs
The faster the change, the more
dangerous the consequences
Any drug that affects water
homeostasis
CHAPTER 11 • ElECTRolyTEs, oTHER MinERAls, And TRACE ElEMEnTs 265
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QUICKVIEW | Potassium
PARAMETER DESCRIPTION COMMENTS
Common reference ranges
Adults and children 3.8–5 mEq/L (3.8–5 mmol/L) Age: >10 days old
Critical value >7 or <2.5 mEq/L (>7 or <2.5 mmol/L) Acute changes more dangerous than
chronic abnormalities; Depends on
serum pH
Natural substance? Yes Most abundant cation; 98% in
intracellular uid
Inherent activity? Yes Control of muscle and nervous tissue
excitability, acid–base balance,
intracellular uid balance
Location
Storage 98% in intracellular uid
Secretion/excretion Mostly secreted by distal nephron Some via GI tract secretion
Major causes of…
High results
Associated signs and symptoms Mostly cardiac EKG changes, bradycardia,
Low results Decreased intake or increased loss Usually a combination of the two or
Associated signs and symptoms Affects primarily cardiac system Table
After insult, time to…
Initial elevation or positive result Hours to years, depending on
Peak values Hours to years, depending on
Normalization Days, if renal function is normal Faster with appropriate treatment
Drugs often monitored with test Diuretics, ACE inhibitors,
Causes of spurious results Hemolyzed samples (falsely elevated) High potassium content in
Renal failure (GFR <10 mL/min) Especially with increased intake and
concurrent acidemia
hypotension, cardiac arrest
concurrent alkalemia
11-7
Acute changes can be life- threatening
chronicity
chronicity
Some drugs are administered
amphotericin B, angiotensin receptor
antagonists, cisplatin, trimethoprim
as potassium salts; be aware of
potassium- sparing medications
erythrocytes
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